Hsu Wei-Chung, Wang Jung-Der, Hsu Chuan-Jen, Lee Shiann-Yann, Yeh Te-Huei
Department of Otolaryngology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan.
Acta Otolaryngol. 2004 May;124(4):459-63. doi: 10.1080/00016480310000584.
Although the mutation in the Gap Junction Beta 2-encoding gap junction protein connexin 26 (Cx26) has been related to hereditary non-syndromic deafness and maturation of cochlear development, the physiological role of Cx26 in the cochlear lateral wall remains unclear. It has been suggested to be responsible for the recycling of K+ in the endolymph and for maintenance of the endocochlear potential (EP). In noise-induced hearing loss, alterations in the EP and the K+ concentration in endolymph have been observed. Thus Cx26, which is widely expressed in the cochlear lateral wall, may play a role in the mechanism of acoustic trauma.
We used a rat model of noise-induced hearing impairment to detect changes in Cx26 expression in the cochlear lateral wall. By means of immunofluorescent staining and Western blotting, we investigated whether Cx26 was involved in the pathophysiological mechanism of acoustic trauma.
The results indicated that abundant Cx26 protein was found on fibrocytes of the spiral ligament in the cochlear lateral wall. Protein extract of cochlear lateral wall expressed Cx26 with a molecular weight of approximately 21 kDa. After noise exposure, with an increasing threshold of the auditory brainstem response (ABR) of approximately 54.2 +/- 21.8 dB SPL, the expression of Cx26 protein increased significantly (p < 0.05) as revealed by semi-quantitative analysis from Western blotting.
Cx26 protein was present in the cochlear lateral wall of rats and was upregulated when the ABR threshold shifted after intense noise exposure. Cx26 protein was involved in the pathogenesis of acoustic trauma.
尽管编码缝隙连接蛋白连接蛋白26（Cx26）的缝隙连接β2发生突变与遗传性非综合征性耳聋以及耳蜗发育成熟有关，但Cx26在耳蜗外侧壁的生理作用仍不清楚。有人认为它负责内淋巴中钾离子的再循环以及维持内淋巴电位（EP）。在噪声性听力损失中，已观察到EP和内淋巴中钾离子浓度的改变。因此，在耳蜗外侧壁广泛表达的Cx26可能在声损伤机制中起作用。
我们使用噪声性听力损伤大鼠模型来检测耳蜗外侧壁Cx26表达的变化。通过免疫荧光染色和蛋白质印迹法，我们研究了Cx26是否参与声损伤的病理生理机制。
结果表明，在耳蜗外侧壁螺旋韧带的纤维细胞上发现了丰富的Cx26蛋白。耳蜗外侧壁的蛋白质提取物表达分子量约为21 kDa的Cx26。噪声暴露后，随着听性脑干反应（ABR）阈值升高约54.2±21.8 dB SPL，蛋白质印迹法的半定量分析显示Cx26蛋白的表达显著增加（p<0.05）。
Cx26蛋白存在于大鼠耳蜗外侧壁，在强烈噪声暴露后ABR阈值改变时上调。Cx26蛋白参与了声损伤的发病机制。
